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[Abstract Title]. - Society for Neuroscience

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Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 292.14/SS27<br />

Topic: F.02.f. Fear and aversive learning and memory<br />

Support: NSC96-2752-B-006-001-PAE<br />

<strong>Title</strong>: A late expression of brain-derived neurotrophic factor in the amygdala is required <strong>for</strong> the<br />

maintenance of long-term fear memory<br />

Authors: L.-C. OU 1 , S.-H. YEH 2 , *P.-W. GEAN 2 ;<br />

1 Inst. Basic Med. Sci., 2 Dept Pharmacol, Natl. Cheng-Kung Univ., Tainan 70101, Taiwan<br />

<strong>Abstract</strong>: In many instances, increase in neuronal activity can elicit a biphasic secretion of a<br />

modulator. The initial release of the modulator triggers the induction of synaptic plasticity<br />

whereas the second phase rein<strong>for</strong>ces the efficacy of synaptic transmission and the growth of<br />

dendrites and axons. Here we show that fear conditioning induces a second peak of brain-derived<br />

neurotrophic factor (BDNF) expression at 12 h post-conditioning. Fluorescent<br />

immunohistostaining confirmed that BDNF expression was increased at 1 and 12 h after<br />

conditioning and returned to baseline at 30 h after conditioning. Mature BDNF level was<br />

similarly increased at 1 and 12 h after fear conditioning. Pre-training administration of TrkB IgG<br />

or K252a impaired fear memory in a test carried out 1 day after training. By contrast, TrkB IgG<br />

or K252a infusion at 9 h after fear conditioning, which did not affect memory retention measured<br />

at 1 day after training, impaired memory when the rats were tested 7 days post-training. Fear<br />

conditioning induced a significant increase in Zif268 expression in the amygdala 12 h after fear<br />

training and the increase was completely blocked by TrkB-IgG infused 9 h post-training.<br />

Growth-associated protein 43 (GAP-43), a marker of newly <strong>for</strong>med synapses, in the amygdala<br />

was increased 7 days after fear conditioning. The change in GAP-43 was completely blocked by<br />

pre-training or 9 h post-training infusion of TrkB-IgG. These results suggest that the second peak<br />

of BDNF expression in the amygdala is responsible <strong>for</strong> the persistence of fear memory.<br />

Disclosures: L. Ou, None; P. Gean , None; S. Yeh, None.<br />

Poster<br />

292. Acetylcholine, Neurotrophins, and Cognition<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 292.15/SS28<br />

Topic: F.02.f. Fear and aversive learning and memory

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